Arterial blood gas analysis clinical scenario.pptx

Arterial blood gas analysis

1. A R TERIAL BLOOD GAS ANALYSIS Dr.Rajkumar S MD DM EDAIC Life is a struggle, not against sin, not against money, power... but against hydrogen ions.- H.L. Mencken

2. Acid Base Disorder Initial Chemical Change Compensatory Response Respiratory Acidosis ↑ PCO2  ↑HCO3- Respiratory Alkalosis ↓ PCO2 ↓ HCO3- Metabolic Acidosis ↓ HCO3- ↓ PCO2 Metabolic Alkalosis ↑ HCO3- ↑ PCO2 DISORDERS

3. Compensation or the Secondary Responses

4. Rule of same direction In simple acid base disorder HCO 3 and PaCO 2 compensatory changes are in the same direction HCO 3 leads to HCO 3 leads to PaCO 2 PaCO 2 This will bring pH towards normal although not to normal Change in opposite direction or not equal to expected suggestive of mixed disorder

5. Compensatory Responses 1 . Compensatory responses never return the pH to normal or overshoot . 2 . The basis of compensatory responses is to maintain the PCO2/[HCO3-] ratio. 3 . Therefore, the direction of the compensatory response is always the same as that of the initial change. 4 . Compensatory response to respiratory disorders is two-fold; a fast response due to cell buffering(acute) and a significantly slower response due to renal adaptation (chronic). 5 . Compensatory response to metabolic disorders involves only an alteration in alveolar ventilation. 6 . Metabolic responses cannot be defined as acute or chronic in terms of respiratory compensation because the extent of compensation is the same in each case.

6. A 20 year old primipara with severe protracted vomiting p r esents to you i n a co n f u sed and irrit a ble st a t e . ABG revealed pH – 7.6, PCO2 -

7. Metabolic Alkalosis

8. Meta b olic Alk a losis Associated with H y poka l em i a and hypochloremia Ventricular arrhythmias Hypercarbia, although compensation rarely results in PaCO 2 >55 mmHg.

9. Meta b olic Alk a losis Under normal circumstances, alkalosis should never develop because the kidney is excellent at excreting excess bicarbonate. Causes Saline responsive (urine chloride <15mEq/L) Vomiting/Gastric suction Diuretics (K + ) Multiple transfusion Saline resistant (urine chloride>20mEq/L) Hyperaldosteronism Cushing syndrome

10. Initiating Factors Maintenance Factors   1. Loss of hydrogen ions from GI 2. Exogenous addition of alkali 3. Transcellular H+ shift 4. Contraction alkalosis 1. Reduced ECV – decreased GFR and increased absorption of HCO3- 2. Hypokalemia Saline Responsive 1. Mineralocorticoid excess 2. Severe Hypokalemia   Hypokalemia Saline Unresponsive    

11. Meta b olic Alk a losis Clinical features CNS: Neuromuscular excitability, paresthesia, light headache CVS : Hypotension,cardiac arrhythmias RS: Compensatory hypo-ventilation

12. Meta b olic Alk a los i s Treatment Treat the underlying cause Saline responsive alkalosis Adequate correction of volume, IV isotonic saline H1 inhibitor or PPI to decrease gastric secrection Avoid exogenous sources of alkali such as NaHCO 3 infusion,

13. Meta b olic Alk a losis If alkalosis is due to diuretics, dose reduction may be required, KCL supplementation, spironolactone or carbonic anhydrase inhibitor. Saline resistant metabolic acidosis Needs specific treatment of underlying causes (surgical treatment of pitutary tumor or adrenal adenoma in cushing syndrome) Supportive treatment such as spiranolactone

14. Treatment Saline - Responsive metabolic alkalosis Re-expand volume with Normal Saline ( Primary Therapy) Supplement with Potassium to treat hypokalemia (alkalosis associated with severe hypokalemia will be resistant to volume resuscitation until K is repleted ) H+  blockers or PPIs if vomiting/NG suction to prevent further losses in H+ ions Discontinue diuretics Acetazolamide if NS contraindicated due to CHF. (Monitor for hypokalemia) HCl or NH4Cl in emergency. ( HCl can cause hemolysis, NH4Cl should not be used in liver disease) Hemodialysis in patients with marked renal failure

15. Saline – Unresponsive metabolic alkalosis ( Mineraldocorticoid excess) Surgical removal of mineralocorticoid producing tumor Aldosterone inhibitor ACE inhibitor. Discontinue steroids Potassium repletion (only intervention needed to treat the alkalosis)

16. Type 1 DM patient who missed his last three doses of insulin presents with vomiting, abdominal pain and deep sig h ing b r ea t hing. ABG revealed p H - 7 . 1, Pa O 2 - 8 8 mm H g , HCO 3 - 8 mEq/L, and PaCO 2 – 20 mmHg. Na – 140 mEq/L, Cl – 106 mEq/L and urine ketone bodies were positive.

17. Meta b olic Aci d osis Metabolic acidosis, characterized by hypobicarbonatemia (<21 mEq/L) and by an acidemic pH (<7.35). Metabolic acidosis occurs as a consequence of buffering by bicarbonate of endogenous or exogenous acid loads or as a consequence of abnormal external loss

18. Pathophysiology of Metabolic Acidosis Loss of base HCO 3 via GI tract Over production of metabolic acids in the body Ingestion or infusion of acid or potential acids Failure of H + excretion by kidney

19. Meta b olic Aci d osis Causes of high anion gap metabolic acidosis DKA Alcoholic ketoacidosis Lactic acidosis Methanol poisoning Salicylate poisoning Ethlylene glycol poisoning

20. Meta b olic Aci d o sis Causes of normal anion gap acidosis Diarrhoea RTA Acetazolamide Pancreatic fistula

21. Meta b olic Aci d os i s Clinical features RS : Kussumal breathing CVS: Arrhythmias, decrease in response to inotropes, secondary hypotension CNS: Headache, confusion, lethargy

22. ANION GAP When acid is added to the body, the [H+] increases and the [HCO3-] decreases. In addition, the concentration of the anion, which is associated with the acid, increases. This change in the anion concentration is termed the anion gap . Na + Unmeasured cations = Cl- + HCO3-  + Unmeasured anions   Anion gap = [Na] – ([Cl-] + [HCO3-]) =12 ± 4 meq /L Unmeasured cations - calcium, magnesium, gamma globulins ,potassium Unmeasured anions - negatively charged plasma proteins (albumin), sulphate , phosphates, lactate , other organic anions

23. ANION GAP If the anion of the acid added to plasma is Cl- , the anion gap will be normal HCl + NaHCO3    → NaCl + H2CO3 → CO2 + H2O Replacement of extracellular HCO3- by Cl- ; there is no change in the anion gap, since the sum of Cl-] + [HCO3-] remains constant If the anion of the acid is not Cl- (e.g. lactate, β- hydroxybutyrate ), the anion gap will increase   HA  +  NaHCO3    → NaA +  H2CO3  → CO2 + H2O ,

24. Elevated Anion Gap (>16 meq ) Normal Anion Gap (8-16 meq) Increased Endogenous production: Ketoacidosis (Alcohol, Starvation, DKA) Lactic Acidosis Uremia Loss of Bicarbonate: Diarrhea Carbonic anhydrase inhibitors Type 2 RTA (proximal) Pancreatic ileostomy Pancreatic, biliary, intestinal fistula Exogenous Administration : ammonium chloride or HCL Decreased Renal Acid Excretion: Type 1(distal) ,4 RTA Renal Failure Intoxications: Methanol, Ethylene Glycol, Paraldehyde, Salicylates, INH Miscellaneous : Hyperkalemia Recovery from DKA

25. Meta b olic Aci d osis - T re a tment Treat the underling cause Alkali therapy Correct volume status and electrolyte imbalance

26. Meta b olic Aci d osis - T re a tment Alkali therapy Amount of HCO 3 required = (desired HCO 3 -actual HCO 3 )×0.5× body weight in kg Carbicarb- generates bicarbonate rather than CO 2

27. Treating Severe Metabolic Acidosis The ideal treatment - Correction of the underlying cause. When urgency dictates more rapid correction, treatment is based on clinical considerations, supported by lab evidence. The best measure of the level of metabolic acidosis is the Standard Base Excess (SBE) because it is independent of PCO 2 . If it is decided to administer bicarbonate- the SBE and the size of the treatable space are used to calculate the dose required.

28. Calculating the Bicarbonate Dose. Dose ( mEq ) = 0.3  x  Wt (kg) x SBE ( mEq /L)     This assumes that the treatable compartment is about 30% of the body, i.e., about 21 liters of 70 kg pt. Our intention is to normalize the extracellular fluid, which is 20% of the body (about 14 liters). But, because the injected bicarbonate also equilibrates to some extent with the intracellular fluid, the "treatable volume" is larger.

29. Use Half the Calculated Dose The full dose returns the metabolic disturbance to about zero. It is usual to give about half the dose which returns the metabolic disturbance about half way back towards normal, i.e., about half way to the zero line.

30. Reasons for caution about administering the full calculated dose of bicarbonate: 1. Injected into Plasma Volume. The bicarbonate is injected initially into the 3 liter plasma volume instead of the calculated 21 liters of treatable volume (it does not cross the cell membrane to enter the two liters of red cells.) So initially- the dose hugely "over-treats" this small compartment. 2. Causes Respiratory Acidosis. For each 100 mEq of bicarbonate- about 2.24 liters of carbon dioxide has to be exhaled, equivalent to ten minutes normal co2 production. Half Hco3- dose corrects the metabolic disturbance half way but produces a transient respiratory acidosis.

31. 3. Raises Intracellular PCO 2 . CO 2 which is produced enters the cells freely, unlike the bicarbonate ions which have been administered. Therefore, the added PCO 2 inside tends to cause the intracellular fluid to become more acid. However this change may be insignificant. 4.Metabolic Alkalosis: Once the underlying pathology causing the metabolic acidosis is corrected, then the bicarbonate therapy will be responsible for a residual iatrogenic metabolic alkalosis.

32. 5. Subsequent Residual Changes. Sodium Ions and subsequent hypernatremia . Osmolarity : The hypernatremia will increase the osmolarity of the extracellular fluid. In combination with other therapy, such as intravenous glucose, this hyperosmolarity may be critical and cause coma. In neonates, rapid infusion of bicarbonate may cause intracranial hemorrhage.

33. Treatment for Lactic Acidosis Identification of the primary illness and   therapy directed toward correction of that disturbance. Type A lactic acidosis- Restoration of tissue oxygen delivery through hemodynamic and/or respiratory support. Reduce further lactate production and allow metabolism of excess lactate to HCO3- . Unlike other forms of metabolic acidosis, the use of sodium bicarbonate in lactic acidosis is controversial, particularly in patients with circulatory and respiratory failure Raising the arterial pH may improve tissue perfusion, by reversing acidemia induced vasodilatation impaired cardiac contractility may diminish the risk of serious arrhythmias.

34. Treatment Diabetic Ketoacidosis The major goals of treatment are 1.rapid fluid volume expansion, 2.correction of hyperglycemia and hyperketonemia, 3.prevention of hypokalemia during treatment, and 4.identification and treatment for any associated bacterial infection Bicarb replacement: If pH < 7.1 and/or cardiac instability present

35. Alcoholic Ketoacidosis Chronic alcohol abuse with recent history of binge drinking, little or no food intake, and persistent vomiting. Characterized by elevated serum ketone levels, high anion gap and normal or only slightly high plasma glucose

36. Treatment Establish ABCs . If the patient's mental status is diminished, consider administration of oxygen, thiamine, dextrose, and naloxone. Hydration with 5% dextrose in normal saline (D5NS) Carbohydrate and fluid replacement reverse the pathophysiologic derangements by increasing serum insulin levels and suppressing the release of glucagon and other counter-regulatory hormones. Dextrose stimulates the oxidation of NADH and aids in normalizing the NADH/NAD+ ratio. Fluids alone do not correct AKA as quickly as fluids and carbohydrates together. Insulin contraindicated - life threatening hypoglycemia (patient’s endogenous insulin levels rise with carbohydrate and fluid repletion) Bicarbonate only given if pH < 7.1, and acidosis not responding to IVF.

37. Patient with a history of overdosing on her sleeping pills presents in a drowsy state with sluggish respiration. ABG revealed pH – 7.1, HCO 3 – 28 mEq/L, PaCO 2 – 72 mmHg and PaO 2 of 78 mmHg.

38. Res p iratory Aci d osis Characterized by hypercarbia (PaCO 2 ≥ 45 mm Hg) and low pH (<7.35), occurs because of a decrease in minute alveolar ventilation Respiratory acidosis may be either acute, without compensation by renal or chronic, with compensation A reduction in minute ventilation may be due to an overall decrease an increase in production of carbon dioxide (V CO2 )

39. Res p iratory Aci d osis Because of the lung’s excellent capacity to excrete excess CO2, increases in PCO2 are always due to hypoventilation and never to increased CO2 production. Decreases in minute ventilation may occur Central ventilatory depression by drugs Central nervous system injury Increased work of breathing Airway obstruction Neuromuscular dysfunction.

40. Res p iratory Aci d osis Increases in dead space volume occur with COPD Pulmonary embolism Consolidations Mucus plugs or foreign body

41. Res p iratory Aci d osis Clinical features Hypercapnia causes neurological features - anxiety, headache, confusion, psychosis, hallucination & coma Mild to moderate chronic Hypercapnia may cause sleep disturbance, loss of memory, daytime somnolence, personality changes, impairment of coordination, tremors and myoclonic jerks

42. Symptoms Symptoms are caused by acute respiratory acidosis & not by chronic respiratory acidosis. Usually neurologic abnormalities. Initial symptoms - headache, blurry vision, restlessness, and anxiety Progressive - to tremors, asterixis, delirium, and somnolence or coma (CO2 narcosis). Severe hypercapnia increases CBF and CSF pressure. Signs of raised ICP such as papilledema may be seen. Acute respiratory acidosis promotes a greater fall in CSF pH than acute metabolic acidosis . Neurologic abnormalities are seen often. In chronic respiratory acidosis, the CO2 accumulates at a much slower rate, allowing renal compensation to return the arterial pH and ultimately CSF pH toward normal. Therefore neurologic abnormalities are RARE

43. T re a tment of Res p iratory Aci d osis Identify and treat the underlying cause Establish patent airway to restore OXYGENATION Oxygen therapy Mechanical ventilation - hyperventilate

44. A 26 year old male with septic shock is on volume control ventilation since the last 4 hours. ABG reveals pH – 7.8, HCO 3 – 14 mEq/L, PaCO 2 – 22 mmHg, PaO 2 – 250mmHg.

45. Res p iratory Alk a losis Respiratory alkalosis, characterized by hypocarbia (PaCO 2 ≤ 35 mmHg) and an alkalaemic pH (>7.45) Results from an increase in minute ventilation that is greater than that required to excrete metabolic CO 2 production.

46. Res p iratory Alk a losis Respiratory alkalosis may be a sign of pain, anxiety, hypoxemia, central nervous system disease or systemic sepsis Development of spontaneous respiratory alkalosis in a previously normo-carbic patient requires prompt evaluation.

47. Respiratory Alkalosis Characterized by elevated arterial pH, hyperventilation resulting in a low pCO2 and a usually compensatory decrease in plasma HCO3- concentration. It is very commonly induced by Stressors. STRESSORS - anxiety, pain, and infection stimulates the CNS leading to hyperventilation. Other common causes - hypoxemia, sepsis, liver failure and PE. Aspirin intoxication is an interesting cause of respiratory alkalosis which can also cause an elevated anion gap acidosis

48. CNS stimulation Hypoxemia or tissue hypoxia Chest Receptors stimulation        1. Flail Chest        2. Hemothorax        3. PE          Miscellaneous disorders

49. Res p iratory Alk a losis Most frequently encountered acid base disorder, since it occurs in normal pregnancy and high altitude Anxiety or pain induced hyperventilation Excessive mechanical ventilation

50. Res p iratory Alk a losis Clinical features Light headache, tingling of the extremities, circumoral anaesthesia, headache, shortness of breath and chest wall tightness

51. Res p iratory Alk a losis Treatment of respiratory alkalosis per se is often not required. The most important steps are recognition and treatment of the underlying cause.

52. Summ a ry ABG analysis requires a thorough understanding of acid- base physiology There are no shortcuts Always correlate with the clinical scenario Just trying to correct any derangement from the normal values is not enough Correct the underlying cause

53. Treatment Treat the underlying cause: oxygen, diuretics, etc. For anxious patient: reassurance, rebreathing into paper bag (raises the inspired PCO2). Teach breath holding techniques during episodes. If intubated, reduce minute ventilation Usually self limited since muscles weakness will suppress ventilation. If the PaCO2 is corrected rapidly in patients with chronic respiratory alkalosis, metabolic acidosis may develop due to the previous compensatory drop in serum bicarbonate .

54. Mixed Acid Base Disorders Occur when - more than one primary acid base disturbance present simultaneously. Frequently seen in hospitalized - critically ill pts

55. The Delta Ratio (∆/∆) Used in the assessment of elevated anion gap metabolic acidosis to determine if a mixed acid base disorder is present. Delta ratio = ∆ Anion gap/∆ [HCO3-] or (AG – 12) (24 - [HCO3-])

56. Delta ratio   Assessment Guidelines      < 0.4     Hyperchloremic normal anion gap acidosis       < 1   High AG & normal AG acidosis (Ex. lactic acidosis with severe diarrhea)     1 to 2   Pure Anion Gap Acidosis Lactic acidosis: average value 1.6 DKA more likely to have a ratio closer to 1 due to urine ketone loss         > 2   High AG acidosis and a concurrent metabolic alkalosis or a pre-existing compensated respiratory acidosis

57. Delta Ratio The elevation in the anion gap usually exceeds the fall in the plasma [HCO3- ] In lactic acidosis, for example, the ∆/∆ ratio averages 1.6:1. In ketoacidosis, the ratio is usually close to 1:1 -The loss of ketoacids anions (ketones) lowers the anion gap and tends to balance the effect of intracellular buffering. - Anion loss in the urine is less in lactic acidosis because the associated state of marked tissue hypoperfusion usually results in little or no urine output.

58. Delta Ratio A delta-delta value below 1:1 indicates - a greater fall in [HCO3-] as in mixed metabolic acidosis - a combined elevated anion gap acidosis and a normal anion gap acidosis(lactic acidosis with severe diarrhea) - the additional fall in HCO3- is due to further buffering of an acid that does not contribute to the anion gap A value above 2:1 indicates - a lesser fall in [HCO3-] - explained by another process that increases the [HCO3-],i.e. a concurrent metabolic alkalosis or chronic respiratory acidosis

59. When to suspect a mixed acid base disorder: 1. The expected compensatory response does not occur. 2. Level of compensation is inadequate or too extreme. 3. Whenever the PCO2 and [HCO3-] becomes abnormal in the opposite direction. 4. pH is normal but PCO2 or HCO3- is abnormal 5. In anion gap metabolic acidosis, if the change in bicarbonate level is not proportional to the change of the anion gap. More specifically, if the delta ratio is greater than 2 or less than 1. 6. In simple acid base disorders, the compensatory response should never return the pH to normal. If that happens, suspect a mixed disorder.

60. Mixed metabolic disorders 1. Anion Gap and Normal Anion Gap Acidosis . In patients with a delta ratio less than 1 Reduction in bicarbonate is greater than it should be, relative to the change in the anion gap  implicating - another process also present requiring buffering by HCO3-, i.e a concurrent NAGA. Example: Lactic acidosis superimposed on severe diarrhea. Progressive Renal Failure DKA during treatment Type IV RTA and DKA

61. 2. Anion Gap Acidosis and Metabolic Alkalosis In patients with a delta ratio greater than 1, which signifies a reduction in bicarbonate less than it should be, relative to the change in the anion gap. The presence of another process functioning to increase the bicarbonate level without affecting the anion gap, i.e. metabolic alkalosis. Examples: Lactic acidosis, uremia, or DKA – with actively vomiting / NG Suction. Patient with lactic acidosis or DKA given sodium bicarbonate therapy.

62. 3. Normal Anion Gap Acidosis and Metabolic Alkalosis Difficult to diagnose Both low HCO3- and low PCO2 move back toward normal when metabolic alkalosis develops. Also, unlike elevated anion gap acidosis, the anion gap will not indicate the presence of the acidosis. Example: In patients who are vomiting and with diarrhea

63. Mixed respiratory and Resp –met disorders Rule of thumb: When the PCO2 is elevated and the [HCO3-] reduced, respiratory acidosis and metabolic acidosis coexist. When the PCO2 is reduced and the [HCO3-] elevated, respiratory alkalosis and metabolic alkalosis coexist The above examples both produce very extreme acidemia or alkalemia and are relatively easy to diagnose. However more often, the disorder is quite subtle. Ex- In cases of metabolic acidosis, the HCO3- is low and PCO2 low. If the PCO2 is normal or not adequately reduced, this may indicate a subtle coexisting respiratory acidosis.

64. Chronic Respiratory Acidosis with superimposed Acute Respiratory Acidosis Acute exacerbation of COPD secondary to acute pneumonia COPD patient with worsening hypoventilation secondary to oxygen therapy or sedative administration Chronic Respiratory Acidosis and Anion Gap Metabolic Acidosis COPD patient who develops shock and lactic acidosis Chronic Respiratory Acidosis and Metabolic Alkalosis Pulmonary insufficiency and diuretic therapy COPD patient treated with steroids or ventilation

65. Respiratory Alkalosis and Metabolic Acidosis Salicylate intoxication Gram negative sepsis Acute cardiopulmonary arrest Severe pulmonary edema It is impossible to have more than one respiratory disorder in the same mixed disorder(i.e. concurrent respiratory alkalosis and respiratory acidosis)

66. THANK YOU

67. Thank you for listening